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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The physiologic factors involved in vaseopressin (ADH) release and action are reviewed with emphasis on the interaction between osmotic and volume stimuli to the discharge of ADH. Abnormalities in reception of stimuli to ADH release, and in the impaired synthesis and release of ADH, are reviewed in relation to the causes of diabetes insipidus, and information on the biochemical changes which have been described in patients with nephrogenic diabetes insipidus is also discussed. We summarize the pathologic lesions and associated diseases found in 54 of our patients with diabetes insipidus. Criteria for establishing the diagnosis of diabetes insipdus are reviewed with emphasis on the dehydration test, including the importance of measuring plasma osmolality at the conclusion of water deprivation. Treatment of diabetes insipidus is briefly discussed with emphasis on the use of DDAVP and oral agents. The syndrome of inappropriate ADH secretion (SIADH) is reviewed including our experience with 39 patients. The differential diagnosis of SIADH, including the value of water loading and the measurement of ADH levels, is discussed. We comment on treatment of these patients including the use of investigational drugs. Lastly, we review the pharmacologic features and clinical relevance of some drugs which alter the release and action of ADH.
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PMID:Pathophysiologic and pharmacologic alterations in the release and action of ADH. 81 77

A physiological investigation on an outbreak of diuresis syndrome in commercial broiler breeder hens was carried out. Daily water consumption increased 4-fold and daily manure wet weight increased two-fold in affected hens. 2. The syndrome did not have a genetic basis. It was associated with kidney dysfunction which, once acquired, was not alleviated by changing the diet, the drinking water, or the environment. Diuresis ceased when water intake was restricted and returned when water was again made freely available. 3. The syndrome was not caused by nephrogenic diabetes insipidus or diabetes mellitus. Key changes in kidney function associated with diuresis included: increased urine flow, decreased urine osmolality, reduced glomerular filtration rates, increased fraction of the glomerular filtration rate excreted as urine and decreased urinary hydrogen ion concentrations. 4. Preliminary histopathological findings and the physiological patterns of kidney dysfunction indicated that the diuresis syndrome was associated with permanent kidney damage, probably caused by the Arkansas strain of infectious bronchitis virus.
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PMID:Physiological evaluation of diuresis in commercial broiler breeders. 276 79

Direct measurement of plasma AVP and indirect assessment of antidiuretic activity during standard dehydration tests were made in 21 polyuric and polydipsic patients to establish the efficacy of each method in determining the cause of polyuria. Patients with acquired nephrogenic diabetes insipidus (e.g. diabetes mellitus, renal failure, hypercalcaemia) were excluded from the study. Cranial diabetes insipidus was diagnosed by plasma AVP responses to osmotic stimulation during infusion of hypertonic 5% saline which were subnormal in 13 patients, 4 of whom had undetectable plasma AVP and 3 who had reduced but osmoregulated AVP release. Standard water deprivation tests confirmed cranial diabetes insipidus in all but 2 patients who were diagnosed as partial nephrogenic diabetes insipidus. The remaining 8 patients had normal, osmoregulated AVP secretion; the cause of their polyuria was determined by their renal response to desmopressin. Two patients had nephrogenic diabetes insipidus and 6 had primary polydipsia. The majority of polyuric patients could be accurately diagnosed by carefully performed dehydration tests. We suggest that direct measurements of plasma AVP during osmotic stimulation are only necessary to distinguish mild forms of cranial from nephrogenic diabetes, or to define precisely the characteristics of AVP secretion.
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PMID:A comparison of diagnostic methods to differentiate diabetes insipidus from primary polyuria: a review of 21 patients. 665 43

We report on a 65-year-old female patient with an A-kappa multiple myeloma diagnosed on the grounds of bone pain, anemia and extremely elevated erythrocyte sedimentation rate (ESR). Eight years prior to admission to the Clinic of Haematology the patient started to excrete a considerable amount of urine (4-6 liters per 24 hrs) with low specific gravity and to experience hardly controllable thirst. The disorder was specified in a specialised endocrinologic clinic as diabetes inspidus with ambiguous aetiology. The administered treatment with adiuretin had a small effect. A course of cyclophosphamide and glucocorticosteroids was started after myeloma was diagnosed--this had a considerable effect on the polyuria and polydipsia; the specific gravity of the urine increased. This effect, as well as the proven light chain proteinuria in the patient, leads to the interpretation of the early complaints of the patient as onset of the underlying disease in the form of nephrogenic diabetes insipidus--a rare light chain tubular syndrome.
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PMID:Nephrogenic diabetes insipidus--prodromal phase of multiple myeloma. 760 96

Hereditary diabetes insipidus can occur in two forms: the first, referred to as central diabetes insipidus, is responsive to vasopressin whereas the second, termed nephrogenic diabetes insipidus, is resistant to treatment. Recent advances in molecular genetics have contributed to elucidate the pathogenesis of these affections. Familial central diabetes insipidus depicts two unsimilar illnesses. The first, characterized by an autosomal dominant transmission, is of delayed onset and worsens progressively all through life. It is related to a heterozygous mutation of the vasopressin precursor gene mainly involving either the sequence encoding for the signal peptide or the one encoding for neurophysin II, the hormone carrier protein. Mutations described to date are responsible for impairment of vasopressin precursor transportation and processing. Therefore mutant protein accumulates in the posterior pituitary which is involved in the persistant bright spot seen on magnetic resonance imaging. The second illness or Wolfram syndrome, autosomal recessive, associates obligatory features: insulin-dependant diabetes, bilateral optic atrophy and more inconstantly: diabetes insipidus, deafness, genito-urinary and neuropsychiatric disturbances. The cause of this syndrome, still unknown, may involve mitochondrial ADN mutations. Familial nephrogenic diabetes insipidus, of neonatal onset, are mainly X-linked and associated to mutations in the V2 receptor gene. About 60 mutations have been described until now. Some rare cases, transmission of which is autosomal recessive, result from homozygous mutations of aquaporin 2 gene, a water channel involved in the water reabsorption in the renal collecting duct. Other mutations will be probably discovered in future. In conclusion, familial diabetes insipidus constitutes an interesting pathogenic model because it may be explained by impairment of vasopressin gene precursor as well as by abnormalities of renal receptor or post receptor mechanisms of the hormone.
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PMID:[Congenital diabetes insipidus. Recent advances in molecular genetics]. 868 70

Nephrogenic diabetes insipidus (DI) secondary to chronic urinary tract obstruction is a rare disease. The exact cause is unknown but it is likely that increased collecting duct pressures cause damage to the tubular epithelium, resulting in insensitivity to the action of arginine-vasopressin (AVP). A 77-year-old man complaining of polyuria and polydipsia was treated with alpha glucosidase inhibitor under the impression of polyuria due to diabetes mellitus. But his symptoms did not improve. Water deprivation and AVP administration study revealed that the patient had nephrogenic DI. Urinary tract obstruction due to an enlarged prostate was suggested as a principal cause of nephrogenic DI. The patient underwent transurethral resection of the prostate and bilateral subcapsular orchiectomy. After surgery, the urine osmolarity was normalized and the patient became symptom-free. We report a case of nephrogenic DI due to obstructive uropathy which was cured by surgery eliminating obstruction.
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PMID:A case of nephrogenic diabetes insipidus caused by obstructive uropathy due to prostate cancer. 1073 36

To investigate the hypothesis that diabetes induces nephrogenic diabetes insipidus, we studied the urine-concentrating ability in response to vasopressin (AVP) in 12 patients with insulin-dependent diabetes mellitus (IDDM) and 12 nondiabetic controls. Subjects were euglycemic-clamped, and after oral water loading, AVP was infused intravenously for 150 min. AVP induced a greater (P<0.001) rise in urine osmolality in controls (67.6+/-10.7 to 720+/-31.1 mosmol/kg, P<0.001) than in IDDM patients (64.3+/-21.6 to 516.7+/-89.3 mosmol/kg, P<0.001). Urinary aquaporin-2 concentrations after AVP infusion were higher in controls (611.8+/-105.6 fmol/mg creatinine) than in IDDM (462.0+/-94.9 fmol/mg creatinine, P = 0. 003). Maximum urine osmolality in IDDM was inversely related to chronic blood glucose control, as indicated by Hb A(Ic) (r = -0.87, P = 0.002). To test the hypothesis that improved glycemic control could reverse resistance to AVP, 10 IDDM subjects with poor glycemic control (Hb A(Ic) >9%) were studied before (B) and after (A) intensified glycemic control. Maximum urine osmolality in response to AVP increased with improved glycemic control (B, 443.8+/-49.0; A, 640.0+/-137.2 mosmol/kg, P<0.001), and urinary aquaporin-2 concentrations after AVP increased from 112.7 +/-69 to 375+/-280 fmol/mg creatinine (P = 0.006), with improved glycemic control. Poorly controlled IDDM is associated with reversible renal resistance to AVP.
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PMID:Renal resistance to vasopressin in poorly controlled type 1 diabetes mellitus. 1089 35

Aldose reductase (ALR2) is thought to be involved in the pathogenesis of various diseases associated with diabetes mellitus, such as cataract, retinopathy, neuropathy, and nephropathy. However, its physiological functions are not well understood. We developed mice deficient in this enzyme and found that they had no apparent developmental or reproductive abnormality except that they drank and urinated significantly more than their wild-type littermates. These ALR2-deficient mice exhibited a partially defective urine-concentrating ability, having a phenotype resembling that of nephrogenic diabetes insipidus.
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PMID:Aldose reductase-deficient mice develop nephrogenic diabetes insipidus. 1091 67

The finding of a polyuropolydispsic syndrome should prompt a complete biological investigation of its etiology. If polyuria can be a minor sign as in psychiatric disorder, it can also be the first manifestation of diabetes mellitus but also central diabetes insipidus, the latter linked to cerebral tumors, metastases in the hypothalamus, granulomatous disease, but also nephrogenic diabetes insipidus such as chronic renal disease or autoimmune disease. Intracellular dehydration is the major risk in case of a polyuropolydipsic syndrome. Prognosis depends on the capacity to maintain water balance through an intact thirst mechanism. After a brief review of the majority of causes of diabetes insipidus, we propose a diagnosis algorithm to easily make the diagnosis.
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PMID:[How to explore... insipidus polyuropolydipsia syndrome]. 1564 41

Renal toxicity of long-term lithium therapy is a common problem. Nephrogenic diabetes insipidus is the most frequently encountered complication, but often remains unrecognised because of the rather benign symptoms. We present a patient with long-term lithium therapy who developed life-threatening hypernatraemia due to insufficient oral fluid intake after elective spinal surgery. Careful daily substitution of up to 25 l of hypotonic fluids led to full recovery within 9 days. Nephrogenic diabetes insipidus should always be considered in lithium-treated patients undergoing elective surgery in order to avoid severe hypernatraemia.
Exp Clin Endocrinol Diabetes 2006 Nov
PMID:Severe hypernatraemia due to nephrogenic diabetes insipidus - a life-threatening side effect of chronic lithium therapy. 1717 43


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